Prevalence and etiology of altered liver tests: A population‐based survey in a Mediterranean town

Gaspare Maria Pendino, Andrea Mariano, Pasquale Surace, Carmelo Antonio Caserta, Maria Teresa Fiorillo, Angela Amante, Stefania Bruno, Carmelo Mangano, Irene Polito, Fulvia Amato, Rodolfo Cotichini, Tommaso Stroffolini, Alfonso Mele, ACE Collaborating Group – 19 April 2005 – Serum biochemical liver tests (LTs) (ALT, AST, GGT) and platelet counts are often used to screen for chronic liver disease. Population‐based data on abnormal LTs in Mediterranean areas are lacking.

Peginterferon alfa‐2b plus ribavirin treatment in children and adolescents with chronic hepatitis C

Stefan Wirth, Heidrun Pieper‐Boustani, Thomas Lang, Antje Ballauff, Ulrike Kullmer, Patrick Gerner, Philip Wintermeyer, Andreas Jenke – 19 April 2005 – Peginterferon plus ribavirin is standard therapy for adults with chronic hepatitis C. As no data are available for children, the aim of the study was to evaluate the efficacy and tolerability of peginterferon alfa‐2b in combination with ribavirin in chronically infected children. Genotypes, alanine aminotransferase levels, and different routes of viral transmission were considered.

A key role for autoreactive B cells in the breakdown of T‐cell tolerance to pyruvate dehydrogenase complex in the mouse

Amanda J. Robe, John A. Kirby, David E. J. Jones, Jeremy M. Palmer – 19 April 2005 – The key immunological event in the pathogenesis of the autoimmune liver disease primary biliary cirrhosis is breakdown of T‐cell self‐tolerance to pyruvate dehydrogenase complex (PDC). The mechanism resulting in this breakdown of tolerance remains unclear.

Interaction between the HCV NS3 protein and the host TBK1 protein leads to inhibition of cellular antiviral responses

Motoyuki Otsuka, Naoya Kato, Masaru Moriyama, Hiroyoshi Taniguchi, Yue Wang, Narayan Dharel, Takao Kawabe, Masao Omata – 19 April 2005 – The persistent nature of hepatitis C virus (HCV) infection suggests that HCV encodes proteins that enable it to overcome host antiviral responses. Toll‐like receptor 3 (TLR3)‐mediated signaling, which recognizes the double‐stranded RNA that is produced during viral replication and induces type I interferons, including interferon β (IFN‐β), is crucial to the host defense against viruses.

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